lupus

摘要： Neuroinflammation plays a critical role in the pathological process of multiple neurological disorders and pathological pain conditions.GPR109A,a Gi protein-coupled receptor,has emerged as an important therapeutic target for controlling inflammation in various tissues and organs.In this review,we summarized current data about the role of GPR109A in neuroinflammation.Specifically,we focused on the pharmacological features of GPR109A and signaling pathways used by GPR109A to ameliorate neuroinflammation and symptoms in Alzheimer’s disease,Parkinson’s disease,multiple sclerosis,stroke,and pathological pain conditions.

摘要： Systemic lupus erythematosus(SLE)is an autoimmune disease with multisystemic features and a variety of clinical characteristics.Typical clinical manifestations of SLE include alopecia,oral ulcers,cutaneous lesions,arthritis,renal injury,and cardiac damage.[1]Cardiac involvement is one of the common complications of SLE,which is mostly asymptomatic with only approximately 10%of cardiac injury patients experiencing symptoms such as shortness of breath and arrhythmia.However,cardiogenic shock is rare,especially as the initial manifestation of SLE.[2]Herein,we report a case of a 15-year-old male who presented with cardiogenic shock and was eventually diagnosed with SLE.

摘要： 抗磷脂抗体综合征(Antiphospholipid syndrome,APS)是由抗磷脂抗体引起的,以反复动脉、静脉血栓,习惯性流产及血小板减少为主要临床表现的一组临床综合征,属于自身免疫性疾病,原因不明,近一半病例患有系统性红斑狼疮(Systemic lupus erythematosus,SLE)[1]。迄今为止,仍然没有确切有效的调节免疫的治疗方法[2]。

摘要： 足细胞内陷性肾小球病(podocytic infolding glomeru⁃lopathy,PIG)在10年前作为一种新的疾病被提出,其是一种罕见的基于特征性组织病理学表现的诊断。其特征是足细胞膜内陷到肾小球基底膜,电镜下可见微球和(或)微管[1]。已报道的病例大多数来自亚洲,PIG最常与系统性红斑狼疮(systemic lupus erythematosus,SLE)等自身免疫性疾病相关。本文报道1例PIG合并干燥综合征的老年女性患者,供临床参考。

摘要： BACKGROUND Studies have suggested that atrial fibrillation(AF)in patients with rheumatic diseases(RD)may be due to inflammation.determine morbidity and mortality associated with AF in hospitalized patients with RD.METHODS The National inpatient sample database from October 2015 to December 2017 was analyzed to identify hospitalized patients with RD with and without AF.A subgroup analysis was performed comparing outcomes of AF among different RD.RESULTS The prevalence of AF was 23.9%among all patients with RD(n=3949203).Among the RD subgroup,the prevalence of AF was highest in polymyalgia rheumatica(33.2%),gout(30.2%),and pseudogout(27.1%).After adjusting for comorbidities,the odds of having AF were increased with gout(1.25),vasculitis(1.19),polymyalgia rheumatica(1.15),dermatopolymyositis(1.14),psoriatic arthropathy(1.12),lupus(1.09),rheumatoid arthritis(1.05)and pseudogout(1.04).In contrast,enteropathic arthropathy(0.44),scleroderma(0.96),ankylosing spondylitis(0.96),and Sjorgen’s syndrome(0.94)had a decreased association of AF.The mortality,length of stay,and hospitalization costs were higher in patients with RD having AF vs without AF.Among the RD subgroup,the highest mortality was found with scleroderma(4.8%),followed by vasculitis(4%)and dermatopolymyositis(3.5%).CONCLUSION A highest association of AF was found with gout followed by vasculitis,and polymyalgia rheumatica when compared to other RD.Mortality was two-fold higher in patients with RD with AF.

摘要： cqvip:系统性红斑狼疮(Systemic lupus erythematosus,SLE)是一种慢性、累及多系统多器官的自身免疫性疾病,通常好发于青春期和更年期之间的女性,临床表现多样,具有显著的异质性。疾病可致重要脏器损害,诊断不及时或治疗不当可危及患者生命[1]。多种因素综合作用,包括遗传、环境、雌激素、免疫耐受的破坏等导致B细胞功能亢进、多种自身抗体生成、炎性细胞因子及免疫调节功能失衡等,引起免疫系统的紊乱,引发了SLE的发病。

摘要： 系统性红斑狼疮(Systemic lupus erythematosus,SLE)是一种慢性、累及多系统多器官的自身免疫性疾病,通常好发于青春期和更年期之间的女性,临床表现多样,具有显著的异质性。疾病可致重要脏器损害,诊断不及时或治疗不当可危及患者生命[1]。多种因素综合作用,包括遗传、环境、雌激素、免疫耐受的破坏等导致B细胞功能亢进、多种自身抗体生成、炎性细胞因子及免疫调节功能失衡等,引起免疫系统的紊乱,引发了SLE的发病。

摘要： 近日,上海交通大学医学院附属仁济医院风湿病学研究所沈南教授团队综合利用表观遗传学、三维基因组学及规律成簇间隔短回文重复(clustered regularly interspaced short palindromic repeats,CRISPR)技术,发现定位于基因间的rs2431697所在的增强子通过特别的染色体三维结构在单核细胞内特异性参与调控miR-146a表达,且不同等位基因可差异性地调控系统性红斑狼疮(systemic lupus erythematosus,SLE)致病基因的表达。

摘要： Systemic lupus erythematosus(SLE)is a systemic autoimmune disease characterized by abnormal cellular and humoral immune responses and excessive autoantibody production.The precise pathologic mechanism of SLE remains elusive.The advent of single-cell RNA sequencing(scRNA-seq)enables unbiased analysis of the molecular differences of cell populations at the single-cell level.We used scRNA-seq to profile the transcriptomes of peripheral blood mononuclear cells from an SLE patient compared with a healthy control(HC).A total of 16,021 cells were analyzed and partitioned into 12 distinct clusters.The marker genes of each cluster and the four major immune cell types(B cells,CD4+T cells,CD8+T cells,myeloid cells,and NK cells)were determined.Moreover,several genes involved in antigen processing and presentation through MHCII were highly enriched.GO enrichment analyses revealed abnormal gene expression patterns and signaling pathways in SLE.Of note,pseudotime analysis revealed that there was a different lineage hierarchy in the peripheral blood mononuclear cells(PBMCs)of the SLE patient,indicating that the cell states were substantially altered under disease conditions.Our analysis provides a comprehensive map of the cell types and states of the PBMCs of SLE patients at the single-cell level for a better understanding of the pathogenesis,diagnosis,and treatment of SLE.

摘要： BACKGROUND Interferons(IFNs)are characterized by a wide range of biological effects,which justifies their potential therapeutic use in several pathologies,but also elicit a wide array of adverse effects in almost every organ system.Among them,renal involvement is probably one of the most complex to identify.CASE SUMMARY We describe four cases of kidney damage caused by different IFN formulations:IFN-β-related thrombotic microangiopathy,IFN-β-induced systemic lupus erythematosus,and two cases of membranous nephropathy secondary to pegylated-IFN-α2B.In each case,we carefully excluded any other possible cause of renal involvement.Once suspected as the casual relationship between drug and kidney damage,IFN treatment was immediately discontinued.In three cases,we observed a complete and persistent remission of clinical and laboratory abnormalities after IFN withdrawal,while the patient who developed thrombotic microangiopathy,despite IFN withdrawal and complement-inhibitor therapy with eculizumab,showed persistent severe renal failure requiring dialysis.CONCLUSION This case series highlights the causal relationship between IFN treatment and different types of renal involvement and enables us to delineate several peculiarities of this association.